Re-entrant ventricular tachycardia as a complication of ablation of idiopathic ventricular premature beats from the right outflow tract: a case report.

We report an unusual case of non-sustained ventricular tachycardia (NSVT) from the epicardial part of the right ventricular outflow tract (RVOT). A 37-year-old woman who underwent in 2006 an ablation for idiopathic ventricular premature beats (VPBs) from the RVOT presented with pre-syncopal NSVT in 2016. A cardiac workup showed no coronary disease, normal biventricular function, and no enhancement on cardiac magnetic resonance imaging. A metabolic positron emission tomography scan excluded inflammation. Biopsies revealed normal desmosomal proteins. An endocardial mapping revealed an area of low voltage potential (<0.5 mV) at the antero-septal aspect of the RVOT corresponding to the initial site of ablation from 2006. Activation mapping revealed poor prematurity and pace-mapping showed unsatisfactory morphologies in the RVOT, the left ventricle outflow tract and the right coronary cusp. An epicardial map revealed a low voltage area at the antero-septal aspect of the RVOT with fragmented potentials opposite to the endocardial scar. Pace-mapping demonstrated perfect match. An NSVT was induced and local electrocardiogram showed mid-diastolic potentials. Ablation was applied epicardially and endocardially without any complication. The patient was arrhythmia free at 4-year follow-up. Cardiac workup allowed to exclude specific conditions such as arrhythmogenic cardiomyopathy, tetralogy of Fallot, sarcoidosis, or myocarditis as a cause for NSVT from the RVOT. The epi and endocardial map showed residual scar subsequent to the first ablation which served as substrate for the re-entrant NSVT. This is the first case which describes NSVT from the epicardial RVOT as a complication from a previous endocardial ablation for idiopathic VPB

In vivo measurements of atrial repolarization alternans based on standard pacemaker technology

It has been shown that repolarization alternans, a beat-to-beat alternation in action potential duration, enhances dispersion of repolarization above a critical heart rate and promotes susceptibility to ventricular arrhythmias. It is unknown whether repolarization alternans is measurable in the atria using standard pacemakers and whether it plays a role in promoting atrial fibrillation. In this work, atrial repolarization alternans amplitude and periodicity are studied in a sheep model of pacing-induced atrial fibrillation. Two pacemakers, each with one right atrial and ventricular lead, were implanted in 4 male sheep after ablation of the atrioventricular junction. The first one was used to deliver rapid pacing for measurements of right atrial repolarization alternans and the second one to record a unipolar electrogram. Atrial repolarization alternans appeared rate-dependent and its amplitude increased as a function of pacing rate. Repolarization alternans was intermittent but no periodicity was detected. An increase of repolarization alternans preceding episodes of non-sustained atrial fibrillation suggests that repolarization alternans is a promising parameter for assessment of atrial fibrillation susceptibility

Intermittent atrial tachycardia facilitates atrial fibrillation by a shortening of activation recovery interval

Introduction: We recently observed in a chronic ovine model that a shortening of action potential duration (APD) as assessed by the activation recovery interval (ARI) may be a mechanism whereby pacing-induced atrial tachycardia (PIAT) facilitates atrial fibrillation (AF), mediated by a return to 1:1 atrial capture after the effective refractory period has been reached. The aim of the present study is to evaluate the effect of long term intermittent burst pacing on ARI before induction of AF.Methods: We specifically developed a chronic ovine model of PIAT using two pacemakers (PM) each with a right atrial (RA) lead separated by ∼2cm. The 1st PM (Vitatron T70) was used to record a broadband unipolar RA EGM (800 Hz, 0.4 Hz high pass filter). The 2nd was used to deliver PIAT during electrophysiological protocols at decremental pacing CL (400 beats, from 400 to 110ms) and long term intermittent RA burst pacing to promote electrical remodeling (5s of burst followed by 2s of sinus rhythm) until onset of sustained AF. ARI was defined as the time difference between the peak of the atrial repolarization wave and the first atrial depolarization. The mean ARIs of paired sequences (before and after remodeling), each consisting of 20 beats were compared.Results: As shown in the figure, ARIs (n=4 sheep, 46 recordings) decreased post remodeling compared to baseline (86±19 vs 103±12 ms, p<0.05). There was no difference in atrial structure as assessed by light microscopy between control and remodeled sheep.Conclusions: Using standard pacemaker technology, atrial ARIs as a surrogate of APDs were successfully measured in vivo during the electrical remodeling process leading to AF. The facilitation of AF by PIAT mimicking salvos from pulmonary veins is heralded by a significant shortening of ARI

Myocardial extracellular volume by T1 mapping: a new marker of arrhythmia in mitral valve prolapse.

We aimed to evaluate the relationship between mitral annular disjunction (MAD) severity and myocardial interstitial fibrosis at the left ventricular (LV) base in patients with mitral valve prolapse (MVP), and to assess the association between severity of interstitial fibrosis and the occurrence of ventricular arrhythmic events. In MVP, MAD has been associated with myocardial replacement fibrosis and arrhythmia, but the importance of interstitial fibrosis remains unknown. In this retrospective study, 30 patients with MVP and MAD (MVP-MAD) underwent cardiovascular magnetic resonance (CMR) with assessment of MAD length, late gadolinium enhancement (LGE), and basal segments myocardial extracellular volume (ECVsyn). The control group included 14 patients with mitral regurgitation (MR) but no MAD (MR-NoMAD) and 10 patients with normal CMR (NoMR-NoMAD). Fifteen MVP-MAD patients underwent 24 h-Holter monitoring. LGE was observed in 47% of MVP-MAD patients and was absent in all controls. ECVsyn was higher in MVP-MAD (30 ± 3% vs 24 ± 3% MR-NoMAD, p < 0.001 and vs 24 ± 2% NoMR-NoMAD, p < 0.001), even in MVP-MAD patients without LGE (29 ± 3% vs 24 ± 3%, p < 0.001 and vs 24 ± 2%, p < 0.001, respectively). MAD length correlated with ECVsyn (rho = 0.61, p < 0.001), but not with LGE extent. Four patients had history of out-of-hospital cardiac arrest; LGE and ECVsyn were equally performant to identify those high-risk patients, area under the receiver operating characteristic (ROC) curve 0.81 vs 0.83, p = 0.84). Among patients with Holter, 87% had complex ventricular arrhythmia. ECVsyn was above the cut-off value in all while only 53% had LGE. Increase in ECVsyn, a marker of interstitial fibrosis, occurs in MVP-MAD even in the absence of LGE, and was correlated with MAD length and increased risk of out-of-hospital cardiac arrest. ECV should be includedin the CMR examination of MVP patients in an effort to better assess fibrous remodelling as it may provide additional value beyond the assessment of LGE in the arrhythmic risk stratification

Learning influences host choice in tsetse

A learning capacity for feeding is described in many insect species including vectors of diseases, but has never been reported in tsetse flies (Diptera, Glossinidae), the cyclic vectors of human (sleeping sickness) and animal trypanosomoses in Africa. Repeated feeding on the same host species by a disease vector is likely to increase the within-species disease-transmission risk, but to decrease it between species

Brugada syndrome in childhood: a potential fatal arrhythmia not always recognised by paediatricians. A case report and review of the literature

We report on a youngster followed by his paediatrician from birth until 14 years of age for premature beats, most likely of ventricular origin. The sudden death of his sister provoked a re-assessment of his electrocardiograms (ECG), resulting in the diagnosis of Brugada syndrome and the subsequent implantation of a cardioverter defibrillator. This syndrome is a well known entity in adult cardiology, first described by Brugada and Brugada in 1992. It is considered to be the second most common cause of death in young adults after road traffic accidents. In children, however, the Brugada syndrome is not well known and we believe to be certainly underdiagnosed

The use of participatory methods in the evaluation of health surveillance systems

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